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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxytocin concentrations were determined in baboon (Papio anubis) corpora lutea, and the effect of oxytocin on dispersed luteal cell progesterone production was evaluated. Oxytocin concentrations increased significantly from an early luteal phase value of 2.1 +/- 1.1 ng/gm to a peak concentration of 18.1 +/- 4.3 ng/gm wet weight in midluteal phase corpora lutea. Corpora albicantia and ovarian stroma had comparatively low oxytocin concentrations. Reverse-phase high-pressure liquid chromatography of corpora lutea extracts gave a peptide peak (retention time, 17.25 min) similar to a standard oxytocin peak. Plasma oxytocin levels, which were significantly higher in the ovarian vein draining a corpus luteum than in the contralateral side or the femoral vein, declined significantly after luteectomy. Oxytocin was localized by immunocytochemical methods in luteal cells. In the early luteal phase oxytocin (4 to 800 mU; 1 mU is equivalent to 2 ng) inhibited basal and human chorionic gonadotropin-stimulated progesterone production by dispersed luteal cells, but in the late luteal phase 200 to 800 mU oxytocin inhibited only human chorionic gonadotropin-stimulated progesterone output. Oxytocin did not affect luteal cell progesterone production in the midluteal phase. Thus oxytocin is present in corpora lutea, can be localized in the luteal cells, is probably produced locally, and may modulate luteal cell progesterone production.
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PMID:Baboon corpus luteum oxytocin: an intragonadal peptide modulator of luteal function. 336

To detect antigens in the plasma of pregnant women that were not found in nonpregnant untreated normal women or males, highly sensitive immunodiffusion techniques with hyperimmune rabbit antiserum were used. The number of pregnancy-associated plasma constituents increased as pregnancy progressed in the 165 patients studied, with all 4 constituents usually seen in the third trimester. The 60 males and 111 nonpregnant women studied did not show any of these antigens. There were significant differences between second and third trimester reactions. (p less than .001). None of the antigens represented human chorionic gonadotropin, human placental lactogen, oxytocin, C-reactive protein, oxytocinase, alkaline phosphatase, or esterase. One of these constituents is present during combined estrogen-progesterone therapy.
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PMID:Antigenic constituents in pregnancy plasma which are undetectable in normal non-pregnant female or male plasma. 462 19

The review article summarizes the results obtained in the author's laboratory during the last few years concerning the action of number of neurohormones such as ACTH, vasopressin, oxytocin, TRH and TRH analogues, human chorionic gonadotropin (HCG) LH-RH, gastrin and gastrin C-terminal fragments and cholecystokinin octapeptide on certain behavioural reactions and brain transmitters. The results obtained suggests that in some of the behavioural reactions elicited by these peptide hormones are brought about by modulatory action of these peptide on brain transmitters. These neurohormones, including gastrointestinal peptide hormones have a time dependent, locus and transmitter specific action on the brain function.
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PMID:The effect of neurohormones on the brain and the endocrine system. 611 Mar 9

Continuous cell lines have been established from a variety of biopsy and postmortem species of tumor from patients with small-cell carcinoma of the lung (SCCL) and have been maintained over several years. The medium from the cultures has been assayed for peptide, glycoprotein, and steroid hormones. Significant amounts of 14 hormones including calcitonin, adrenocorticotropin (ACTH), parathormone, luteinizing hormone, chorionic gonadotropin, glucagon, growth hormone, somatostatin, prolactin, beta-endorpin, lipotropin, oxytocin-neurophysin, vasopressin-neurophysin, and estradiol have been demonstrated. Up to ten different hormones have been produced by a single cell line. Most produce ACTH and all evaluated so far produce estradiol. These studies indicate that cells from SCCL have a potential for producing a wide variety of hormones and that this characteristic can be maintained for prolonged periods of culture in vitro.
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PMID:Hormone production by cultures of small-cell carcinoma of the lung. 626 22

Literature on the etiology, diagnosis, and treatment of missed abortion is reviewed. Missed abortion during the 1st 28 weeks of gestation is defined as retention in the uterus of an abortus. The incidence of missed abortion among spontaneous miscarriages is 2.6-9.4%. Etiology of missed abortion is associated with intrauterine infections, severe abnormalities, inhibition of uterine contraction, or impairment of the hormonal balance. Prolonged retention of an abortus can result in fetal maceration or mummification. Clinical manifestations of missed abortion include absence of fetal heart tone, discharge from the breasts and diminution of their size, general fatigue, fever, and sometimes skin itch. Diagnosis of missed abortion is based upon the results of general and gynecologic examinations. Missed abortion is characterized by cessation of growth of the uterus, decrease in cyanosis of the cervix uteri, decrease in urinary excretion of estriol (up to 0-5 mg/day), drastic decrease in excretion of chorionic gonadotropin, decrease in blood level of placental lactogen, and decrease in pregnadiol excretion. Echographic signs of missed abortion during the 1st trimester include absence of heart activity, absence of fetal movements, and changes in the size of the uterus, amniotic cavity, and embryo. The most frequent complications of missed abortion are uterine hemorrhage, infection, and malignant transformation. Treatment of women with missed abortion consists of administration of abortifacient agents and curettage. The most frequently used abortifacient agents are oxytocin in large dosages, intravenous infusions of prostaglandin e2 (PGE2) or single intraamniotic injection of 15-methyl-PGF2alpha. The women with threatening uterine hemmorrage can be subjected to hysterectomy.
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PMID:[Diagnosis and treatment of missed abortion]. 661 58

The effect of a pharmacologic dose of synthetic oxytocin on corpus luteum function was evaluated in rhesus monkeys during normal menstrual cycles, or during menstrual cycles in which the corpus luteum was concomitantly stimulated by injections of human chorionic gonadotropin (hCG). Oxytocin administered by intramuscular injection at a total dose of 4.5 milligrams (2250 I.U.) on Day +6 of the normal luteal phase (Day 0 is the day of the midcycle LH surge) did not change the concentrations of progesterone in the peripheral serum of monkeys or alter the duration of the luteal phase. The same dose of oxytocin, administered to monkeys on Day 22 of menstrual cycles in which hCG was also given on Days 20-22, caused a small, but statistically significant, reduction in serum progesterone values. The results indicate that oxytocin does not alter luteal life span or markedly change blood progesterone concentrations in primates.
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PMID:The effect of oxytocin on the corpus luteum of the monkey. 664 Dec 25

The direct regulation of testis androgen and progestin biosynthesis by neurohypophysial hormones was investigated in a primary culture of rat testis cells. Treatment with arginine vasotocin (AVT; 10(-6) M) over a 10-day period inhibited the human chorionic gonadotropin (hCG)-stimulated testosterone accumulation while enhancing hCG-stimulated progesterone accumulation. Furthermore, treatment with increasing doses (10(-11) - 10(-6) M) of AVT by itself led to dose-dependent increases in the accumulation of pregnenolone (ED50: 8.0 +/- 0.2 X 10(-9) M) and progesterone (ED50: 1.6 +/- 0.3 X 10(-8) M) but not testosterone. Under blockade of pregnenolone metabolism using cyanoketone and spironolactone, AVT, like hCG, stimulated pregnenolone accumulation with an ED50 dose of 5.8 +/- 0.3 X 10(-9) M. Similar effects were observed with several related neurohypophysial hormones, but not with nine unrelated peptides. AVT, arginine vasopressin, and lysine vasopressin were about 100-fold more potent than mesotocin, valitocin, and oxytocin. Pressor (but not antidiuretic or oxytocic)-selective agonists of the neurohypophysial hormones also exerted dose-dependent stimulation of pregnenolone accumulation. Potent pressor (but not oxytocic)-selective antagonistic analogs of the neurohypophysial hormones prevented the AVT-stimulated accumulation of pregnenolone. Thus, the neurohypophysial hormones may exert a direct stimulatory effect on testis pregnenolone and progesterone biosynthesis via putative, pressor-selective recognition sites, and this progestin-stimulatory activity may be partly due to stimulation of steroidogenic steps preceding pregnenolone formation. Since the effective doses of neurohypophysial hormones in vitro are higher than the serum hormone levels, the present results suggest an intratesticular paracrine role for these peptides.
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PMID:Direct regulation of rat testicular steroidogenesis by neurohypophysial hormones. Divergent effects on androgen and progestin biosynthesis. 671 52

Human trophoblast produce GnRH and its precursor, immunologically and chemically identical to those of hypothalamic origin. Placental GnRH stimulates human chorionic gonadotropin secretion by the syncytiotrophoblast. It is known that GnRH analogue has negative effect on early rat pregnancy and may cause abortion through its action on the corpus luteum. A significant reduction of progesterone production was found in pregnant rats treated with GnRH agonist. GnRH caused a significant decrease in the maximal contraction intensity of non-pregnant and pregnant uterine muscle strip, following the action of oxytocin and acetylcholine. It was observed that treatment of pregnant rat with pharmacological doses of GnRH was able to delay parturition. Experimentally, GnRH significantly inhibited the release of placental prostaglandins E and F and thromboxane B 2 in a dose dependent fashion. Maternal circulating GnRH levels at 25-35 weeks of gestation were significantly higher in women who later had post-term pregnancies. In an other study maternal circulating GnRH concentration was found to be significantly lower in four patients who developed preterm labor and delivery. Low doses of GnRH in pregnant rats produced inhibition of postpartum lordosis behavior.
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PMID:GnRH in pregnancy. 893 22

Activin A (beta A-beta A) and activin B (beta B-beta B) are related dimeric proteins that regulate numerous cellular activities. Activin activity is bioneutralized by follistatin, a specific and high-affinity binding protein. Recently, our group developed specific and sensitive enzyme-linked immunosorbent activin assays that do not detect either activin isoform when bound to follistatin, therefore, the assays are specific for biologically relevant ligands. Activin A is measurable in the serum of pregnant women (cross-sectional sample collection), while activin B is not detected in maternal serum. However, activin B is measurable in amniotic fluid and cord blood sera. The purpose of this study was to measure serum activin A, activin B, and follistatin prospectively in longitudinally collected samples during pregnancy. This study design offered observations of relative changes in serum hormone concentration with each person serving as an internal reference. Serum samples were collected bimonthly from seven pregnant women beginning within the second month of gestation, and up to, but not including, the onset of labor. Six of the seven women had normal labor and delivery. One patient required pitocin (an oxytocin agonist) for induction of labor which led to delivery. Activin A, activin B, total follistatin, free follistatin, human chorionic gonadotropin, estradiol, progesterone, FSH, and LH were measured in maternal serum samples using specific assays. Serum activin A levels increased in the final month of pregnancy in the six patients who delivered following normal labor (< 0.78 ng/ml (first trimester) to 1-6 ng/ml (term)). Activin B was not detected in any serum sample (< 0.78 pg/ml). Total serum follistatin (free follistatin, follistatin-activin, and follistatin-inhibin) increased 10- to 45-fold in the final month of pregnancy in four of the women undergoing normal labor (10 ng/ml (first trimester) to 100-450 ng/ml (final month)). Total follistatin was high and variable in two women throughout pregnancy. Total follistatin returned to basal serum concentration in three of the patients during the last 2 weeks of pregnancy. Free follistatin was detected throughout pregnancy (range < 2-35 ng/ml). Free follistatin represented a small percentage of the total follistatin throughout the time of pregnancy and did not rise coincident with the rise in total follistatin. Serum activin A and activin B were not detected during the entire course of pregnancy in the one patient who did not have normal labor and total follistatin did not rise in the last trimester of pregnancy. Gonadotropin and steroid hormones were measured in all patients and were within normative ranges for human pregnancy (inclusive of the non-laboring patient). The results suggest that immunodetectable activin A is present in the third trimester of pregnant women who have normal onset labor. The total follistatin assay results suggest that follistatin-activin (or -inhibin) complexes are upregulated during the third trimester of pregnancy. Importantly, activin A production exceeds the binding capacity of circulating follistatin. Because binding protein free activin A is biologically active we conclude that the activin A detected in late pregnancy is biologically relevant. The findings are consistent with our hypothesis that activin A is an endocrine factor during the last trimester of human pregnancy and may be involved in normal labor.
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PMID:Activin A and follistatin are dynamically regulated during human pregnancy. 907 73

During the second half of the luteal phase, the human corpus luteum becomes responsive to regular luteinizing hormone (LH) pulses. These LH pulses stimulate progesterone secretion tonically, and during this tonic stimulation, additional LH-independent progesterone pulses occur, which are particularly pronounced in women with human chorionic gonadotropin-stimulated luteal function. No progesterone pulses are seen in women suffering from corpus luteum deficiency due to absent LH pulses. The corpus luteum thus has a progesterone pulse generator turned on by gonadotropins but functioning for several hours without further gonadotropic support. This pulse generator appears to be regulated by intraluteal auto-/paracrine mechanisms, which we have investigated in a porcine model using molecular, cellular, and in vivo tools. Luteal oxytocin and progesterone release occurs in tightly coupled pulses. In vivo, oxytocin and prostaglandin F2 alpha(PGF2 alpha) stimulate estradiol and progesterone release and estradiol itself further stimulates progesterone release. Analysis of the different luteal cell compartments (large luteal cells, small luteal cells, fibroblasts) suggests an intraluteal circuit that involves paracrine effects of estradiol, oxytocin, and PGF2 alpha. At the time of luteolysis, the luteotropic effects of estradiol are inhibited by tumor necrosis factor derived from invading macrophages and the intraluteal circuit is thereby disrupted, leading to luteolysis.
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PMID:Regulation of steroid production and its function within the corpus luteum. 961 90


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